From surface to core: does better cooling make a difference after cardiac arrest?

Hypoxic–ischaemic brain injury (HIBI) remains the leading cause of death and disability after out-of-hospital cardiac arrest. Although targeted temperature management has long been considered a cornerstone of neuroprotection, recent evidence has challenged the clinical benefit of therapeutic hypothermia compared with active fever prevention. A recent post-hoc analysis of the TTM-2 trial comparing intravascular cooling (IC) and surface cooling (SFC) in patients treated with hypothermia after cardiac arrest demonstrated superior temperature control with IC, including faster achievement of target temperature, improved maintenance within the therapeutic range, lower rates of post-treatment fever, and less temperature variability compared with SFC. Despite these advantages in cooling performance, no statistically significant improvement in six-month neurological outcomes was observed after adjustment for confounding factors. These findings suggest that greater technical efficiency in delivering hypothermia does not necessarily translate into better patient-centred outcomes. The study highlights the persistent uncertainty surrounding the role of hypothermia in adult HIBI. Experimental evidence indicates that earlier and more rapid cooling may enhance neuroprotection, yet the cooling rates achieved in clinical practice remain substantially slower than those associated with benefit in preclinical models. Consequently, it remains unclear whether the lack of observed benefit reflects limitations of hypothermia itself or shortcomings in its implementation. Current evidence supports guideline recommendations favouring active normothermia and fever prevention after cardiac arrest. Future research should focus on defining optimal strategies for maintaining normothermia and determining whether effective fever control can improve neurological recovery in this population.